44 MAyglothling ED Critical Care.pdf

Care of the Critically Ill in the Emergency Department

You want me to do what???

Julie Mayglothling, MD, FACEP Associate Professor of Emergency Medicine and Surgery

Director, Surgical Trauma ICU Virginia Commonwealth University

Patient Demographics Age/Race

Age 65

ED Length of Stay

McCaig, Adv Data. 2006 Jun 23;(372):1-29

HEALTH POLICY/ORIGINAL RESEARCH

National Trends in Emergency Department Occupancy,2001 to 2008: Effect of Inpatient Admissions

Versus Emergency Department Practice IntensityStephen R. Pitts, MD, MPH, Jesse M. Pines, MD, MBA, Michael T. Handrigan, MD,* Arthur L. Kellermann, MD, MPH

From the Department of Emergency Medicine, Emory University School of Medicine, Atlanta, GA (Pitts); the Center for Health Care Quality, GeorgeWashington University Medical Center, Washington, DC (Pines); the Emergency Care Coordination Center, Office of the Assistant Secretary for

Preparedness and Response, Washington, DC (Handrigan); and the RAND Corporation, Santa Monica, CA (Kellermann).

Study objective: We evaluate recent trends in emergency department (ED) crowding and its potential causes byanalyzing ED occupancy, a proxy measure for ED crowding.

Methods: We analyzed data from the annual National Hospital Ambulatory Medical Care Surveys from 2001 to2008. The surveys abstract patient records from a national sample of hospital EDs to generate nationallyrepresentative estimates of visits. We used time of ED arrival and length of ED visit to calculate mean andhourly ED occupancy.

Results: During the 8-year study period, the number of ED visits increased by 1.9% per year (95% confidenceinterval 1.2% to 2.5%), a rate 60% faster than population growth. Mean occupancy increased even more rapidly,at 3.1% per year (95% confidence interval 2.3% to 3.8%), or 27% during the 8 study years. Among potentialfactors associated with crowding, the use of advanced imaging increased most, by 140%. But advanced imaginghad a smaller effect on the occupancy trend than other more common throughput factors, such as the use ofintravenous fluids and blood tests, the performance of any clinical procedure, and the mention of 2 or moremedications. Of patient characteristics, Medicare payer status and the age group 45 to 64 years accounted forsmall disproportionate increases in occupancy.

Conclusion: Despite repeated calls for action, ED crowding is getting worse. Sociodemographic changes accountfor some of the increase, but practice intensity is the principal factor driving increasing occupancy levels.Although hospital admission generated longer ED stays than any other factor, it did not influence the steeptrend in occupancy. [Ann Emerg Med. 2012;xx:xxx.]

Please see page XX for the Editors Capsule Summary of this article.

0196-0644/$-see front matterCopyright 2012 by the American College of Emergency Physicians.http://dx.doi.org/10.1016/j.annemergmed.2012.05.014

SEE EDITORIAL, P. XXX.

INTRODUCTIONBackground

Since 1992, the number of emergency department (ED)visits in the United States has increased at roughly twice the rateof the population growth,1,2 whereas the number of nonruralEDs has declined by 27%.3 In 2006, the Institute of Medicineconducted a comprehensive review of hospital-based emergencycare and concluded that it is at the breaking point.4 TheInstitute of Medicine cited several factors that contribute to EDcrowding, including relentless growth in ED visits, a shortage of

on-call specialists, and lengthy delays before admitted EDpatients are moved to inpatient beds, a practice commonlyreferred to as boarding. Similar conclusions were reached bythe US General Accountability Office5,6 in 2003 and 2009.

ImportanceED crowding contributes to increased waiting times and

dissatisfaction with care.7 It has also been linked to adverseoutcomes, including delays in the provision of criticaltreatments such as antibiotics for pneumonia and analgesia foracute, painful conditions.8-10 Crowding has been associatedwith higher rates of medical errors, more frequentcomplications, and increased mortality rates among critically illpatients.8,11-16 When ED crowding reaches crisis levels, manyhospitals opt to divert inbound ambulances, a practice thatcontributes to community-wide delays in care for acute

*Current affiliation: Provider Compliance Group, Centers for Medicareand Medicaid Services.

Volume xx, . x : Month Annals of Emergency Medicine 1

n 50,000 patients n 1,000 with ED-LOS > 6 hours n Higher ICU and hospital LOS n Higher ICU and hospital mortality

Patients dont get the same care and the same attention as they do in the ICU

n Blunt trauma patients intubated prehospital or in the ED

n ED LOS is an independent risk factor for pneumonia n Increased 20% for every hour they spent in the ED n Preventative measures may help to decrease risk

Resources

n Most EDs not designed or staffed to provide care beyond initial 30-60 minutes

ED Intensive Care (ED-ICU)

n Bringing the upstairs care, downstairs n Multi-disciplinary n Short stay ICU

n DKA n CHF n Trauma

n Undifferentiated n Same staffing , equipment and support as ICU

Checklists Decrease errors

Decrease variations in practice

Informed Consent

Analgesia

Equipment

Prophylactic Antibiotics? (for transient bacteremia caused by I&D)

Sterilize the field

Is this an Abscess?An abscess is a tender, swollen erythematous nodule with a palpable area of fluctuanceUse ultrasound to distinguish hypoechoic collection of abscess from cobblestoning of cellulitisUse doppler to ensure the collection identified is not vascular and to locate surrounding vascular structures.If ultrasound is not available or results are equivocal, consider needle aspiration to confirm diagnosis [1]

Vascular malformation: history of vascular repair, location near major vessels, exam may demonstrate bruitor thrill. Have a low threshold to use doppler sonography - I&D of AVM is dangerousHerpetic whitlow: vesicular lesion, often on hands, often with history of HSV (oral or genital)Kerion: boggy, tender, elevated scalp nodule in context of tinea infectionHidradenitis suppurativa: recurrent groin, buttocks or axilla furuncles/abscessesI&D not curative andnot recommended as treatment in isolation [2]Myiasis: slowly enlarging lesion, recent travel to tropics, sensation of movement under skinSTI: granuloma inguinale, chancroid, lymphogranuloma venereum if suggestive location and historySporotrichosis: slowly progressive, less painful ulcerative lesion in plant handlers / agriculture workers

Should this abscess be drained in the emergency department?Consider surgical assessment for peri-rectal, hand/palm/sole, nasolabial fold, adjacent to major blood vessel/nerve, verylarge/deep abscess, multiple abscesses, abscess complicating recent surgeryPerianal abscess can be drained in the ED if fluctuant dome is visualized and rectal exam verifies no rectal extension - if uncertain, consider imaging vs. surgical assessment [3]Breast abscess: aspiration is less painful and equally effective [4] [5]For equivocal cases consider warm soaks with or without abx, close observation and indications for immediate return

Emergency Department Incision & Drainage Checklist

Initial Evaluation

Procedure

gloves, face shield, gown drape and gauze skin antiseptic local anesthetic (see anesthesia below) syringe and needle (25-30 gauge)

culture swab (if indicated, see below) packing (if indicated, see below) scalpel (size 11 or 15 blade) curved hemostat or cotton swab

forceps scissors dressing tape

Cellulitis

Abscess

Indicated in these patients [6] History of infective endocarditis Prosthetic cardiac valve or prosthetic material used for cardiac valve repair Cardiac transplant recipients who develop cardiac valvulopathy Unrepaired cyanotic congenital heart disease (CHD) Repaired CHD with prosthetic material for 6 months after procedure Repaired CHD with residual defects at or adjacent to site of prosthetic

device

Antibiotic choice - to be given 30-60 minutes before I&D PO amoxicillin (2g, 50 mg/kg) IM/IV ampicillin (2g, 50 mg/kg),

cefazolin or ceftriaxone (1g, 50 mg/kg) PO PCN allergy cephalexin (2g, 50 mg/kg) or

clindamycin (600 mg, 20 mg/kg) IV PCN allergy cefazolin, ceftriaxone, or clindamycin Concern for MRSA PO clindamycin or IV vancomycin (20 mg/kg)

Expected Benefits: resolution of infection, prevention of worsening infection, relief of painPossible Harms: pain, failure of the procedure requiring repeat procedure, bleeding, scar formationAlternatives: antibiotics, warm soaks, observationOral or parenteral analgesia/anxiolysis prior to beginning procedureProcedural sedation is indicated for an abscess that will be particularly painful to drain or difficult to anesthetize with local/regional techniques, as well as for uncooperative/particularly fearful patients

chlorhexadine or providone iodine [1]Abscess I&D is not a sterile procedure but field is customarily sterilized

ddx

Informed Consent

Analgesia

Equipment

Prophylactic Antibiotics? (for transient bacteremia caused by I&D)

Sterilize the field

Is this an Abscess?An abscess is a tender, swollen erythematous nodule with a palpable area of fluctuanceUse ultrasound to distinguish hypoechoic collection of abscess from cobblestoning of cellulitisUse doppler to ensure the collection identified is not vascular and to locate surrounding vascular structures.If ultrasound is not available or results are equivocal, consider needle aspiration to confirm diagnosis [1]

Vascular malformation: history of vascular repair, location near major vessels, exam may demonstrate bruitor thrill. Have a low threshold to use doppler sonography - I&D of AVM is dangerousHerpetic whitlow: vesicular lesion, often on hands, often with history of HSV (oral or genital)Kerion: boggy, tender, elevated scalp nodule in context of tinea infectionHidradenitis suppurativa: recurrent groin, buttocks or axilla furuncles/abscessesI&D not curative andnot recommended as treatment in isolation [2]Myiasis: slowly enlarging lesion, recent travel to tropics, sensation of movement under skinSTI: granuloma inguinale, chancroid, lymphogranuloma venereum if suggestive location and historySporotrichosis: slowly progressive, less painful ulcerative lesion in plant handlers / agriculture workers

Should this abscess be drained in the emergency department?Consider surgical assessment for peri-rectal, hand/palm/sole, nasolabial fold, adjacent to major blood vessel/nerve, verylarge/deep abscess, multiple abscesses, abscess complicating recent surgeryPerianal abscess can be drained in the ED if fluctuant dome is visualized and rectal exam verifies no rectal extension - if uncertain, consider imaging vs. surgical assessment [3]Breast abscess: aspiration is less painful and equally effective [4] [5]For equivocal cases consider warm soaks with or without abx, close observation and indications for immediate return

Emergency Department Incision & Drainage Checklist

Initial Evaluation

Procedure

gloves, face shield, gown drape and gauze skin antiseptic local anesthetic (see anesthesia below) syringe and needle (25-30 gauge)

culture swab (if indicated, see below) packing (if indicated, see below) scalpel (size 11 or 15 blade) curved hemostat or cotton swab

forceps scissors dressing tape

Cellulitis

Abscess

Indicated in these patients [6] History of infective endocarditis Prosthetic cardiac valve or prosthetic material used for cardiac valve repair Cardiac transplant recipients who develop cardiac valvulopathy Unrepaired cyanotic congenital heart disease (CHD) Repaired CHD with prosthetic material for 6 months after procedure Repaired CHD with residual defects at or adjacent to site of prosthetic

device

Antibiotic choice - to be given 30-60 minutes before I&D PO amoxicillin (2g, 50 mg/kg) IM/IV ampicillin (2g, 50 mg/kg),

cefazolin or ceftriaxone (1g, 50 mg/kg) PO PCN allergy cephalexin (2g, 50 mg/kg) or

clindamycin (600 mg, 20 mg/kg) IV PCN allergy cefazolin, ceftriaxone, or clindamycin Concern for MRSA PO clindamycin or IV vancomycin (20 mg/kg)

Expected Benefits: resolution of infection, prevention of worsening infection, relief of painPossible Harms: pain, failure of the procedure requiring repeat procedure, bleeding, scar formationAlternatives: antibiotics, warm soaks, observationOral or parenteral analgesia/anxiolysis prior to beginning procedureProcedural sedation is indicated for an abscess that will be particularly painful to drain or difficult to anesthetize with local/regional techniques, as well as for uncooperative/particularly fearful patients

chlorhexadine or providone iodine [1]Abscess I&D is not a sterile procedure but field is customarily sterilized

ddxEmergency Department Intubation ChecklisT

Is non-invasive ventilation (CPAP/BiPAP) an option? Is the patient DNI status? Has patient/family consented, if applicable?

! Consider the indication for intubation

Look externally, Evaluate 3-3-2 rule, Mallampati score, Obstruction, Neck MobilityBeard, Obese, No teeth, Elderly, Sleep Apnea / SnoringRestricted mouth opening, Obstruction, Distorted airway, Stiff lungs or c-spineSurgery, Hematoma, Obesity, Radiation distortion or other deformity, Tumor*

! Preoxygenate with high-flow oxygen Difficult laryngoscopy! Assess for Difficult BVM Difficult extraglottic device Difficult cricothyrotomy

If suspected difficult airway and time allows, consider awake technique and/or call for help see awake intubation checklist on page 2! Check for dentures Dentures in for bag-valve-mask, out for laryngoscopy

! Position patientAuditory meatus to suprasternal notch (sheets under neck / occiput / shoulders)Patient's head to operator's lower sternum (bed height)**Torso angle at 30 recommended, especially in obesity or upper GI bleed

! Monitoring equipment

ECGPulse oximetryBlood pressureContinuous end-tidal capnography -verify function with test breath

! IV access Two lines preferable

Equipment Use Broselow tape for sizes in pediatrics

! Suction under patient's shoulder - verify function If suspected soiled airway (blood, vomitus, secretions), suction under each shoulder

! Oral airways Size: Angle of mouth to tragus of ear (usually 80, 90, or 100 mm in adults)! Laryngoscopy blades - verify bulbs Curved and straight / One size larger, one size smaller

! Nasal airways Size: Tip of nose to tragus of ear (usually 26 Fr/6.5 mm, 28/7, or 30/7.5 in adults)

! Laryngoscopy handles - verify power At least two! Ambu bag connected to oxygen Size: approximate nasal bridge, malar eminences, alveolar ridge / Err larger

! Colorimetric capnometer To be used if continuous not available or not functioning! Endotracheal tubes - verify cuffs Variety of sizes ( 8.0 mm preferred in adults to facilitate ICU care)! ETT stylet Straight to cuff, 35 degrees**! ETT securing device Tape if no device available

Drugs Pretreatment agents, if applicable Give as bolus 3 minutes prior to induction, except for fentanyl, which should be the final pretreatment agent, and should be given over 30-60 seconds.

Atropine .02 mg/kg IV or IM (min 0.1 mg, max 1 mg) For infants, especially if receiving succinylcholine

Lidocaine 1.5 mg/kg TBW for reactive airways or increased ICPFentanyl 3 mcg/kg TBW if high BP a concern (aneurysms, dissections, high ICP, severe CAD)

! Paralytic agentSuccinylcholine 2 mg/kg IV 4 mg/kg IM TBWRocuronium 1.2 mg/kg TBWVecuronium 0.3 mg/kg IBW if Roc unavailable

Contraindications to succinylcholineHistory of malignant hyperthermiaBurn or crush injury > 5 days old

Stroke or spinal cord injury > 5 days oldMS, ALS, or inherited myopathyKnown hyperkalemia (absolute)

Renal failure (relative)Suspected hyperkalemia (relative)

! Normal saline flushes! Phenylephrine For post-intubation hypotension100 mcg IV push as needed

At least 3 min or 8 deep breaths if possible, consider NIV if profound hypoxia

! Induction agent

Etomidate 0.3 mg/kg TBWPropofol 1.5 - 3 mg/kg IBW+(.4)(TBW)Ketamine 2 mg/kg IV or 4 mg/kg IM IBWMidazolam 0.2 - 0.3 mg/kg TBWThiopental 3- 6 mg/kg TBW

! Gum elastic bougie

! Difficult airway equipment Cricothyrotomy tools / video laryngoscope / optical stylet fiberoptic scope / Magill forceps if suspected foreign body

Reduce dose if hypotensive

! LMA with lubricant and syringe

! Nasal cannula 5 liters per minute to augment preoxygenation, then 15 liters per minute post-induction to facilitate apneic oxygenation

FAST HUG

FAST HUG

n Feeding n Analgesia n Sedation n Thromboembolic Prophylaxis n Head of Bed Elevation n Ulcer (Stress Ulcer Prophylaxis) n Glucose Control

Analgesia !""#""$%&'()$%'!""*+$),#-'.$,/'0123*4#-'

56,+*1#"

!"#$%&'()*+(,(-*./(011'11&'/#2 3/*45"1#'4(

!6 -045"1#'4(

!6 -

7% 8'1

9:3(;% ?@> AB@? ABC@ ?BAC ABD?

9:3(E!F ?G(4 ?H(4 ?BDA I(ABA? ?BJH ABAJ

;K(4" AB@? ABC@ ?BAC ABD?

9:3(E!F ?G(4 ?H(4 ?BDA I(ABA? ?BJH ABAJ

;K(4"

Sedation

n New SCCM Guidelines on PAD

n Anaglesia first n Light levels of sedation

better than deep levels n Lorazepam and midazolam

higher delirium n Recommend

n RASS (-5 to +4) n SAS (1 to 7)

Thromboembolic Prophylaxis

Head of Bed Elevation

n Decreases rate of VAP n Improved ventilation

30-45

stress Ulcer prophylaxis

14 trials 1720 patients PPI with less UGIB than H2 blockers

Glucose Control

n engl j med 360;13 nejm.org march 26, 2009 1283

The new england journal of medicineestablished in 1812 march 26, 2009 vol. 360 no. 13

Intensive versus Conventional Glucose Control in Critically Ill Patients

The NICE-SUGAR Study Investigators*

ABSTRACT

The NICE-SUGAR study is a collabora-tion of the Australian and New Zealand Intensive Care Society Clinical Trials Group, the George Institute for Interna-tional Health (University of Sydney), the Canadian Critical Care Trials Group, and the Vancouver Coastal Health Research Institute (University of British Columbia). The NICE-SUGAR study writing commit-tee (Simon Finfer, F.R.C.P., F.J.F.I.C.M., Dean R. Chittock, F.R.C.P.C., Steve Yu-Shuo Su, Ph.D., Deborah Blair, R.N., Denise Foster, R.N., Vinay Dhingra, F.R.C.P.C., Rinaldo Bellomo, F.J.F.I.C.M., Deborah Cook, M.D., Peter Dodek, M.D., William R. Henderson, F.R.C.P.C., Paul C. Hbert, M.D., Stephane Heritier, Ph.D., Daren K. Heyland, M.D., Colin McArthur, F.J.F.I.C.M., Ellen McDonald, R.N., Imo-gen Mitchell, F.R.C.P., F.J.F.I.C.M., John A. Myburgh, Ph.D., F.J.F.I.C.M., Robyn Nor-ton, Ph.D., M.P.H., Julie Potter, R.N., M.H.Sc.(Ed.), Bruce G. Robinson, F.R.A.C.P., and Juan J. Ronco, F.R.C.P.C.) assumes full responsibility for the overall content and integrity of the article. Address re-print requests to Dr. Finfer at the George Institute for International Health, P.O. Box M201, Missenden Rd., Sydney NSW 2050, Australia, or at [email protected].

*The Normoglycemia in Intensive Care EvaluationSurvival Using Glucose Al-gorithm Regulation (NICE-SUGAR) study committees and investigators are listed in the Appendix.

This article (10.1056/NEJMoa0810625) was published at NEJM.org on March 24, 2009.

N Engl J Med 2009;360:1283-97.Copyright 2009 Massachusetts Medical Society.

BackgroundThe optimal target range for blood glucose in critically ill patients remains unclear.

MethodsWithin 24 hours after admission to an intensive care unit (ICU), adults who were expected to require treatment in the ICU on 3 or more consecutive days were ran-domly assigned to undergo either intensive glucose control, with a target blood glucose range of 81 to 108 mg per deciliter (4.5 to 6.0 mmol per liter), or conven-tional glucose control, with a target of 180 mg or less per deciliter (10.0 mmol or less per liter). We defined the primary end point as death from any cause within 90 days after randomization.

ResultsOf the 6104 patients who underwent randomization, 3054 were assigned to un-dergo intensive control and 3050 to undergo conventional control; data with regard to the primary outcome at day 90 were available for 3010 and 3012 patients, respec-tively. The two groups had similar characteristics at baseline. A total of 829 patients (27.5%) in the intensive-control group and 751 (24.9%) in the conventional-control group died (odds ratio for intensive control, 1.14; 95% confidence interval, 1.02 to 1.28; P = 0.02). The treatment effect did not differ significantly between operative (surgical) patients and nonoperative (medical) patients (odds ratio for death in the intensive-control group, 1.31 and 1.07, respectively; P = 0.10). Severe hypoglycemia (blood glucose level, 40 mg per deciliter [2.2 mmol per liter]) was reported in 206 of 3016 patients (6.8%) in the intensive-control group and 15 of 3014 (0.5%) in the conventional-control group (P

EDS FAST HUGS

EDS FAST HUGS n Euvolemia n DVT Prophylaxis ***previously T n Stress Ulcer Prophylaxis ***previously U n FiO2 n Analgesia n Sedation n Trending Lactate

n Head of Bed Elevation n Urine Output Assessment

n Glucose Control n Sacrum Sparing (patient positioning)

Euvolemia

EDS FAST HUGS

n E = Euvolemia

n D = DVT prophylaxis

n S = Stress Ulcer prophylaxis

FiO2 CARING FOR THECRITICALLY ILL PATIENT

Association Between Arterial HyperoxiaFollowing Resuscitation From Cardiac Arrestand In-Hospital MortalityJ. Hope Kilgannon, MDAlan E. Jones, MDNathan I. Shapiro, MD, MPHMark G. Angelos, MDBarry Milcarek, PhDKrystal Hunter, MBAJoseph E. Parrillo, MDStephen Trzeciak, MD, MPHfor the Emergency Medicine ShockResearch Network (EMShockNet)Investigators

SUDDEN CARDIAC ARREST IS THEmost common lethal conse-quence of cardiovascular dis-ease. Even if return of sponta-neous circulation (ROSC) from cardiacarrest is achieved, approximately 60%of patients will not survive to hospitaldischarge.1,2 The high mortality is at-tributed to the postcardiac arrest syn-drome,which involves global ischemia-reperfusion injury, myocardialstunning, and anoxic brain injury.3 Therecent success of therapeutic hypother-mia for post-ROSC neuroprotection4,5

has increased momentum for investi-gating post-ROSC factors that can im-prove outcomes.In the search for modifiable post-

ROSC factors, the role of supplemen-tal oxygen, which is often adminis-tered in high concentrations to patientsafter cardiac arrest has come into con-

troversy.6 There is a paradox with oxy-genwhendelivered to the injured brain.Too little oxygen may potentiate an-

oxic injury. Toomuch oxygenmay in-crease oxygen free radical production,possibly triggering cellular injury and

For editorial comment see p 2190.

Author Affiliations: Department of EmergencyMedicine (Drs Kilgannon and Trzeciak), Division ofCritical Care Medicine, Department of Medicine (DrsParrillo and Trzeciak), and Biostatistics Group (DrMilcarek and Ms Hunter), Cooper University Hospi-tal, Camden, New Jersey; Department of EmergencyMedicine, Carolinas Medical Center, Charlotte,North Carolina (Dr Jones); Department of Emer-gency Medicine and Center for Vascular BiologyResearch, Beth Israel Deaconess Medical Center,

Boston, Massachusetts (Dr Shapiro); and Depart-ment of Emergency Medicine, Ohio State University,Columbus (Dr Angelos).Corresponding Author: Stephen Trzeciak, MD,MPH,Cooper University Hospital, One Cooper Plaza, D363,Camden, NJ 08103 ([email protected]).Caring for the Critically Ill Patient Section Editor:Derek C. Angus, MD, MPH, Contributing Editor,JAMA ([email protected]).

Context Laboratory investigations suggest that exposure to hyperoxia after resuscita-tion fromcardiac arrestmayworsen anoxic brain injury; however, clinical data are lacking.

Objective To test the hypothesis that postresuscitation hyperoxia is associated withincreased mortality.

Design, Setting, and Patients Multicenter cohort study using the Project IMPACTcritical care database of intensive care units (ICUs) at 120 US hospitals between 2001and 2005. Patient inclusion criteria were age older than 17 years, nontraumatic car-diac arrest, cardiopulmonary resuscitation within 24 hours prior to ICU arrival, and ar-terial blood gas analysis performedwithin 24 hours following ICU arrival. Patients weredivided into 3 groups defined a priori based on PaO2 on the first arterial blood gasvalues obtained in the ICU. Hyperoxia was defined as PaO2 of 300 mm Hg or greater;hypoxia, PaO2 of less than 60 mm Hg (or ratio of PaO2 to fraction of inspired oxygen!300); and normoxia, not classified as hyperoxia or hypoxia.

Main Outcome Measure In-hospital mortality.

Results Of 6326 patients, 1156 had hyperoxia (18%), 3999 had hypoxia (63%),and 1171 had normoxia (19%). The hyperoxia group had significantly higher in-hospital mortality (732/1156 [63%; 95% confidence interval {CI}, 60%-66%]) com-pared with the normoxia group (532/1171 [45%; 95% CI, 43%-48%]; proportiondifference, 18% [95%CI, 14%-22%]) and the hypoxia group (2297/3999 [57%; 95%CI, 56%-59%]; proportion difference, 6% [95% CI, 3%-9%]). In a model control-ling for potential confounders (eg, age, preadmission functional status, comorbid con-ditions, vital signs, and other physiological indices), hyperoxia exposure had an oddsratio for death of 1.8 (95% CI, 1.5-2.2).

Conclusion Among patients admitted to the ICU following resuscitation from car-diac arrest, arterial hyperoxia was independently associated with increased in-hospitalmortality compared with either hypoxia or normoxia.JAMA. 2010;303(21):2165-2171 www.jama.com

2010 American Medical Association. All rights reserved. (Reprinted) JAMA, June 2, 2010Vol 303, No. 21 2165

Downloaded From: http://jama.jamanetwork.com/ on 03/05/2013

CARING FOR THECRITICALLY ILL PATIENT






















































Trending Lactate

manner at discrete time points over thefirst 72 hrs to serially follow the trend inscores as an indicator of the progressionof disease (26). The addition of lactateclearance in assessing the patients phys-iological reserve and as an indicator ofoutcome has further implications in un-derstanding the progression of sepsis to

multiple organ failure and death in thepre-ICU period.

This study was limited to one urbanED setting with a high level of patientacuity and an ICU admission rate thatnearly doubles the national average (49).Therefore, the stratification of patientsinto lactate clearance groups with the

observed mortality rates should be gen-eralized only with caution to other EDs.Traditional resuscitation end points suchas vital signs fail to definitively addressthe severity of global tissue hypoxia andthus are a poor reflection of the resusci-tation and the development of organ fail-ure and death. Initial serial lactate mea-surements in the presence of SIRS alertthe clinician to the severity of illness andmay be associated with outcome.

CONCLUSIONS

Lactate clearance in the most proxi-mal presentation of severe sepsis and sep-tic shock is associated with improvedmorbidity and mortality rates. This isconsistent with current efforts that em-phasize the importance of identifying andtreating tissue hypoperfusion during thefirst 6 hrs of resuscitation (50). Furtherclinical trials are needed to conclusivelyestablish lactate clearance as a resuscita-tion end point and an outcome measureto be targeted during the most proximalphases of severe sepsis and septic shock.

ACKNOWLEDGMENTS

We thank the nurses and the technicaland administrative support staff in theDepartment of Emergency Medicine atHenry Ford Hospital for their assistancein this study.

REFERENCES

1. Huckabee WE: Abnormal resting blood lac-tate, I. The significance of hyperlactemia inhospitalized patients. Am J Med 1961; 30:833

2. Weil MH, Afifi AA: Experimental and clinicalstudies on lactate and pyruvate as indicatorsof the severity of acute circulatory failure(shock). Circulation 1970; 41:9891001

3. Vitek V, Cowley RA: Blood lactate in the

Table 4. Baseline characteristics, therapy, and outcome between high and low lactate clearance groups

Low Lactate Clearance!10% (n " 31)

High Lactate Clearance!10% (n " 80) p Value

Age, yrs 62.0 # 15.7 66.0 # 17.0 .25Vital signs

Temperature, C 37.4 # 1.4 36.6 # 2.3 .07Heart rate, beats/min 117.6# 20.9 116.6 # 28.8 .87MAP, mm Hg 82.5 # 26.9 74.8 # 23.8 .14CVP, mm Hg 5.3 # 5.9 6.4 # 8.9 .96

Laboratory valuesWBC, per mm3 13.1 # 8.3 15.1 # 10.3 .39Hematocrit, % 33.6 # 8.1 35.2 # 8.0 .35Platelet, per mm3 164,000 # 82,000 220,000 # 119,000 .02a

Prothrombin time, secs 18.2 # 6.9 16.0 # 5.9 .01a

D-Dimer, ng/mL 4903 # 1549 2728 # 3604 .59Creatinine, mg/dL 2.8 # 2.8 2.5 # 1.5 .59Albumin, g/dL 2.6 # 0.8 2.9 # 0.7 .07Total bilirubin, mg/dL 2.7 # 3.3 1.8 # 3.2 .06Base deficit, mmol/L 7.6 # 8.2 8.8 # 7.4 .34pH 7.32 # 0.20 7.33 # 0.18 .86ScvO2, % 50.8 # 11.6 51.6 # 14.3 .87Lactate, mmol/L 7.0 # 5.7 6.9 # 4.2 .28

Therapy, hrsIntravenous fluids, mL

06 2828 # 1947 3572 # 2956 .44772 9200 # 6629 10,246 # 6550 .44

PRBC transfusion, %06 25.8 15.0 .18772 41.9 35.4 .53

Mechanical ventilation, %06 58.1 51.3 .52772 29.0 13.9 .07

Vasopressor, %06 45.2 22.5 .02a

772 61.3 39.2 .04a

Dobutamine, %06 0.0 3.8 .56772 9.7 8.9 .99

OutcomeAPACHE II, hrs 19.4 # 5.8 20.5 # 7.1 .46

6 19.3 # 6.4 17.1 # 6.3 .0912 18.3 # 6.4 14.9 # 6.2 .02a

24 17.2 # 6.5 14.1 # 6.1 .03a

36 16.8 # 6.8 13.1 # 5.8 .01a

48 14.3 # 4.5 12.8 # 6.2 .3460 14.5 # 5.3 12.6 # 5.4 .1872 14.7 # 6.1 12.5 # 5.4 .15

In-hospital mortality rate, % 67.7 32.5 !.001a

30-day mortality rate, % 67.7 37.5 .004a

60-day mortality rate, % 71.0 42.5 .007a

Severe sepsis, % 29.0 55.0 .01a

Lactate, mmol/L 4.8 # 2.9 6.4 # 3.8 .20In-hospital mortality rate, % 55.6 20.5 .03a

Septic shock, % 71.0 45.0 .01a

Lactate, mmol/L 7.9 # 6.4 7.5 # 4.5 .41In-hospital mortality rate, % 72.7 47.2 .06

MAP, mean arterial pressure; CVP, central venous pressure; WBC, white blood cell; ScvO2, centralvenous oxygen saturation; PRBC, packed red blood cell; APACHE, Acute Physiology and ChronicHealth Evaluation.

aStatistically significant, p ! .05.

Figure 1. Kaplan-Meier survival analysis betweenpatients with lactate clearance !10 vs. !10% at6 hrs after emergency department presentation.

1641Crit Care Med 2004 Vol. 32, No. 8

EDS FAST HUGS

n F = FiO2

n A = Analgesia

n S = Sedation

n T = Trending Lactate

Urine Output Assessment

Sacrum Sparing

EDS FAST HUGS

n H = Head of Bed Elevation

n U = Urine Output Assessment

n G = Glucose Control

n S = Sacral Sparing

Frequency?

n ED patients may be dynamic n Cant be too labor intensive

n Every 4 hours? n Every 6 hours? n Every 8 hours?

EDS FAST HUGS n Euvolemia n DVT Prophylaxis

n Stress Ulcer Prophylaxis n FiO2 n Analgesia

n Sedation n Trending Lactate

n Head of Bed Elevation n Urine Output Assessment

n Glucose Control n Sacrum Sparing (patient positioning)

EDS FAST HUGS q6

Questions?

What about care in the ED?

Documents

44 MAyglothling ED Critical Care.pdf